When it comes to body fat, the hormone Insulin is the critical factor. If insulin is up, body fat goes up; if insulin is down, body fat goes down.
To complicate matters even further, it is impossible to determine which comes first! As fat cells grow they tend to develop and promote a general resistance to insulin throughout the body.
Contrary to what you may think, a fat cell cannot expand endlessly; they are able to hold only so much fat!
Like an overflowing cup, when your fat cells are “full,” the excess fat begins spilling over into the blood and gets stored in other tissues including the liver and muscles.
Insulin sends a powerful signal to the fat cell to store fat, which means to pull fat in directly from the blood and to make new fat from glucose.
However, insulin also prevents any fat from leaving, inhibiting the fat-shrinking process of “lipolysis.”
There is a fascinating and even obvious difference between fat cells that are insulin sensitive and continuing to store fat and those that are insulin resistant and “leaking” fat—it’s all about size.
Size Matters
As we gain fat, our fat tissue can grow in two ways:
-
Via an increased number of fat cells (yet the fat cells themselves remain small; this is called “hyperplasia”)
-
A growth in cell size (yet the number of fat cells remains lower; this is called “hypertrophy”).
Larger fat cells have relatively fewer insulin receptors, for their size, than smaller fat cells. Because of this, larger fat cells may not receive sufficient insulin stimulus, and as a result, the larger fat cells experience a degree of fat breakdown despite the presence of insulin attempting to block the process.
This series of events is evidence of a personal fat threshold—a limit to the size of the fat cells (and fat mass, by extension). When a fat cell reaches its maximum dimensions through hypertrophy (which is several times that of the normal fat cell), it attempts to limit further growth; an excellent way to do this is to become resistant to insulin’s growth signal. However, if fat cells can multiply via hyperplasia, they never reach this limit and retain sensitivity.
Importantly, the insulin-resistant fat cell that’s grown beyond its borders not only leaks fat, but because it’s “too big,” it also becomes inflamed, dumping inflammatory proteins into the blood.
In the end, this means that the body is receiving this toxic mix of too much fat and too much inflammation, both of which drive insulin resistance.
Causes of fat cell growth
The first, and likely the worst, fat molecule that makes fat cells grow is called 4-hydroxynonenal
(4-HNE) which is born from the union of a polyunsaturated fat (such as an omega-6 fat) and reactive oxygen molecules (or oxidative stress).
Unfortunately in our modern diets, linoleic acid, the omega-6 fat of interest has increased almost 150% in the last 50 years!!
Linoleic fat is essentially the main fat in all processed and packaged foods and has become a significant part of the fat we store in our fat cells, constituting roughly one quarter of it.
As 4-HNE accumulates, it disrupts the fat cell’s ability to proliferate, forcing it to grow in size rather than number.
The second fat character that disrupts fat cell growth, forcing hypertrophy, is called ceramide 1-phosphate (C1P). Whereas 4-HNE is a consequence of oxidative stress, C1P can be considered more a consequence of inflammation.
Through a series of steps, a cell can create C1P from other innocent fats, but the initial steps are turned on by inflammation signals. However it happens, once C1P accrues to a certain point, it flips the same switches as 4-HNE and the fat cells become limited in their ability to multiply, increasing fat cell insulin resistance.
The larger, fewer fat cells begin leaking not only fat but also proteins called cytokines that promote inflammation. As the fat cells continue leaching these toxic contents into the blood, tissues “downstream” of the fat cells, including the liver and muscle, are the victims. So the problem starts in the fat cells but soon carries over to the liver, muscles, pancreas and even the brain!
Once inflammatory pathways are activated, innocent fats become the dangerous fats called ceramides that actively work against insulin signaling in cells.
Its not inside its on top!
There are typically two “patterns” of fat storage; the difference between these two types of fat storage being specific to the placement of the fat.
-
The gynecoid ,fat pattern is the result of fat stored beneath the skin also known as “subcutaneous fat.” This pattern is typified by fat accumulating on the hips and thighs, with less fat on the upper body and trunk. This is commonly referred to as the ‘pear shape’ and is typically seen with women due to the actions of oestrogen.
-
In contrast, the “android” pattern may have both subcutaneous and visceral fat—meaning fat inside the trunk of the body, surrounding the visceral organs (liver, kidneys, intestines, and heart). This is the typical male fat storage pattern, analogous to the “apple’ body shape. Someone with the android pattern stores most of their body fat right around the middle of the body, fondly referred to as a “beer belly”..
Study after study has shown that storing fat inside the core of the body is harmful as it behaves very differently to the fat stored under the skin.
Apart from the obvious reason of putting pressure on the internal organs thus possibly impeding their function; visceral fat is kilo for kilo more inflammatory than subcutaneous fat.
In an effort to remove the fat from these fat cells and reduce the size of the fat, visceral fat tissue becomes populated with white blood cells (macrophages) whose main job is to clean up cellular messes.
Unfortunately, as an individual continues to accrue visceral fat (due to diet and genetics), the macrophage begins to lose the battle and is itself filled with fat—becoming a “foam cell” .
The foam cells send out inflammatory proteins to bring other macrophages to the area to help; they, too, will become foam cells over time, and the problem will build.
It is fact that carrying too much fat is detrimental, and not just because you can’t fit into your favourite pair of jeans!
Too much fat leads to chronic inflammation which in turn can develop into serious degenerative conditions which will result in a vicious cycle unless the underlying cause is addressed.
Waist to Hip Ratio
One of the easiest ways to determine whether you are an apple or a pear is to compare the girth around the largest part of your belly with the largest part around your hips and then divide the waist number by the hip number
For example if your waist is 76cm and your hips are 96cm, your waist to hip ratio is 0.79.
For men the number should ideally be below 0.9 and for women below 0.8.
In the next blog post we will discuss how to address the issue through changes to the lifestyle and diet.
Resources: Why we get sick: B Bikman
When it comes to body fat, the hormone Insulin is the critical factor. If insulin is up, body fat goes up; if insulin is down, body fat goes down.
To complicate matters even further, it is impossible to determine which comes first! As fat cells grow they tend to develop and promote a general resistance to insulin throughout the body.
Contrary to what you may think, a fat cell cannot expand endlessly; they are able to hold only so much fat!
Like an overflowing cup, when your fat cells are “full,” the excess fat begins spilling over into the blood and gets stored in other tissues including the liver and muscles.
Insulin sends a powerful signal to the fat cell to store fat, which means to pull fat in directly from the blood and to make new fat from glucose.
However, insulin also prevents any fat from leaving, inhibiting the fat-shrinking process of “lipolysis.”
There is a fascinating and even obvious difference between fat cells that are insulin sensitive and continuing to store fat and those that are insulin resistant and “leaking” fat—it’s all about size.
Size Matters
As we gain fat, our fat tissue can grow in two ways:
-
Via an increased number of fat cells (yet the fat cells themselves remain small; this is called “hyperplasia”)
-
A growth in cell size (yet the number of fat cells remains lower; this is called “hypertrophy”).
Larger fat cells have relatively fewer insulin receptors, for their size, than smaller fat cells. Because of this, larger fat cells may not receive sufficient insulin stimulus, and as a result, the larger fat cells experience a degree of fat breakdown despite the presence of insulin attempting to block the process.
This series of events is evidence of a personal fat threshold—a limit to the size of the fat cells (and fat mass, by extension). When a fat cell reaches its maximum dimensions through hypertrophy (which is several times that of the normal fat cell), it attempts to limit further growth; an excellent way to do this is to become resistant to insulin’s growth signal. However, if fat cells can multiply via hyperplasia, they never reach this limit and retain sensitivity.
Importantly, the insulin-resistant fat cell that’s grown beyond its borders not only leaks fat, but because it’s “too big,” it also becomes inflamed, dumping inflammatory proteins into the blood.
In the end, this means that the body is receiving this toxic mix of too much fat and too much inflammation, both of which drive insulin resistance.
Causes of fat cell growth
The first, and likely the worst, fat molecule that makes fat cells grow is called 4-hydroxynonenal
(4-HNE) which is born from the union of a polyunsaturated fat (such as an omega-6 fat) and reactive oxygen molecules (or oxidative stress).
Unfortunately in our modern diets, linoleic acid, the omega-6 fat of interest has increased almost 150% in the last 50 years!!
Linoleic fat is essentially the main fat in all processed and packaged foods and has become a significant part of the fat we store in our fat cells, constituting roughly one quarter of it.
As 4-HNE accumulates, it disrupts the fat cell’s ability to proliferate, forcing it to grow in size rather than number.
The second fat character that disrupts fat cell growth, forcing hypertrophy, is called ceramide 1-phosphate (C1P). Whereas 4-HNE is a consequence of oxidative stress, C1P can be considered more a consequence of inflammation.
Through a series of steps, a cell can create C1P from other innocent fats, but the initial steps are turned on by inflammation signals. However it happens, once C1P accrues to a certain point, it flips the same switches as 4-HNE and the fat cells become limited in their ability to multiply, increasing fat cell insulin resistance.
The larger, fewer fat cells begin leaking not only fat but also proteins called cytokines that promote inflammation. As the fat cells continue leaching these toxic contents into the blood, tissues “downstream” of the fat cells, including the liver and muscle, are the victims. So the problem starts in the fat cells but soon carries over to the liver, muscles, pancreas and even the brain!
Once inflammatory pathways are activated, innocent fats become the dangerous fats called ceramides that actively work against insulin signaling in cells.
Its not inside its on top!
There are typically two “patterns” of fat storage; the difference between these two types of fat storage being specific to the placement of the fat.
-
The gynecoid ,fat pattern is the result of fat stored beneath the skin also known as “subcutaneous fat.” This pattern is typified by fat accumulating on the hips and thighs, with less fat on the upper body and trunk. This is commonly referred to as the ‘pear shape’ and is typically seen with women due to the actions of oestrogen.
-
In contrast, the “android” pattern may have both subcutaneous and visceral fat—meaning fat inside the trunk of the body, surrounding the visceral organs (liver, kidneys, intestines, and heart). This is the typical male fat storage pattern, analogous to the “apple’ body shape. Someone with the android pattern stores most of their body fat right around the middle of the body, fondly referred to as a “beer belly”..
Study after study has shown that storing fat inside the core of the body is harmful as it behaves very differently to the fat stored under the skin.
Apart from the obvious reason of putting pressure on the internal organs thus possibly impeding their function; visceral fat is kilo for kilo more inflammatory than subcutaneous fat.
In an effort to remove the fat from these fat cells and reduce the size of the fat, visceral fat tissue becomes populated with white blood cells (macrophages) whose main job is to clean up cellular messes.
Unfortunately, as an individual continues to accrue visceral fat (due to diet and genetics), the macrophage begins to lose the battle and is itself filled with fat—becoming a “foam cell” .
The foam cells send out inflammatory proteins to bring other macrophages to the area to help; they, too, will become foam cells over time, and the problem will build.
It is fact that carrying too much fat is detrimental, and not just because you can’t fit into your favourite pair of jeans!
Too much fat leads to chronic inflammation which in turn can develop into serious degenerative conditions which will result in a vicious cycle unless the underlying cause is addressed.
Waist to Hip Ratio
One of the easiest ways to determine whether you are an apple or a pear is to compare the girth around the largest part of your belly with the largest part around your hips and then divide the waist number by the hip number
For example if your waist is 76cm and your hips are 96cm, your waist to hip ratio is 0.79.
For men the number should ideally be below 0.9 and for women below 0.8.
In the next blog post we will discuss how to address the issue through changes to the lifestyle and diet.
Resources: Why we get sick: B Bikman